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Medical Forum / Diseases and Disorders / AIDS / October 2005

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Ok Iconclaster you claim HEPATITIS C  is like HIV a nonexistent figment of the imagination

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Gary Stein - 21 Sep 2005 23:44 GMT
Then where are the following 29 articles wrong please anaylize them one at a
time and post your evidence as to why a particular article is mistaken in
it's premises about Hep C.

NATAP - http://www.natap.org

29 RECENT HEPATITIS C ARTICLES posted to NATAP website:
http://www.natap.org

1.     New Hep C Protease Inhibitor  - (09/21/05)
http://www.natap.org/2005/HCV/092105_01.htm

2.     Liver Injury and Changes in Hepatitis C Virus (HCV) RNA Load
Associated with Protease Inhibitor-Based Antiretroviral Therapy for
Treatment-Naive HCV-HIV-Coinfected Patients: Lopinavir-Ritonavir versus
Nelfinavir  - (09/21/05)
http://www.natap.org/2005/HCV/092105_02.htm

3.     PEGINTERFERON a-2b THERAPY IN ACUTE HEPATITIS C: IMPACT OF ONSET AND
DURATION OF THERAPY ON SUSTAINED VIROLOGIC RESPONSE - (09/20/05)
http://www.natap.org/2005/HCV/092005_01.htm

4.     Fatigue & Hypermetabolism in HCV: high HCV RNA may cause fatigue &
interferon appears to reduce fatigue - (09/19/05)
http://www.natap.org/2005/HCV/091905_03.htm

5.     HCV natural history in the west & developing world: The retrospective
and prospective in perspective - (09/19/05)
http://www.natap.org/2005/HCV/091905_02.htm

6.     (Marijuana/Hash) Endocannabinoids and liver disease - review -
(09/19/05)
http://www.natap.org/2005/HCV/091905_01.htm

7.     Impact of Hepatitis C Virus on Immune Restoration in HIV-Infected
Patients Who Start Highly Active Antiretroviral Therapy: A Meta-analysis -
(09/14/05)
http://www.natap.org/2005/HCV/091405_10.htm

8.     Hepatitis C Virus Infection in HIV Type 1-Infected Individuals Does
Not Accelerate a Decrease in the CD4+ Cell Count but Does Increase the
Likelihood of AIDS-Defining Events - (09/14/05)
http://www.natap.org/2005/HCV/091405_09.htm

9.     VA Study: HCV Increases Risk of Death Among HAART-Treated HIV+
Patients by 30-80% - (09/14/05)
http://www.natap.org/2005/HCV/091405_08.htm

10.     Influence of Hepatitis C Virus Infection on HIV-1 Disease
Progression and Response to Highly Active Antiretroviral Therapy -
(09/14/05)
http://www.natap.org/2005/HCV/091405_07.htm

11.     Hepatic steatosis with stavudine in HIV/hepatitis C virus
co-infection - (09/14/05)
http://www.natap.org/2005/HCV/091405_06.htm

12.     Promising Therapy for Human Hepatoma (liver cancer, HCC): Telomerase
Inhibition by GRN163 - (09/13/05)
http://www.natap.org/2005/HCV/091405_05.htm

13.     Single (B or C), dual (BC or BD) and triple (BCD) viral hepatitis in
HIV-infected patients in Madrid, Spain - (09/13/05)
http://www.natap.org/2005/HCV/091405_04.htm

14.     Is Cirrhosis Inevitable in HCV? - (09/13/05)
http://www.natap.org/2005/HCV/091405_03.htm

15.     Insulin resistance is a cause of steatosis and fibrosis progression
in chronic hepatitis C - (09/13/05)
http://www.natap.org/2005/HCV/091405_01.htm

16.     Hepatocellular carcinoma in 40 HIV/HCV-coinfected versus 50
HCV-monoinfected patients. North American HCC in HIV Study Gro (09/09/05)
http://www.natap.org/2005/ias/ias_53.htm

17.     Caucasians Had Better HCV Viral Load Reductions Than
African-Americans During First 3 Days & During Weeks 1-4 After Starting
Peg/RBV (09/09/05)
http://www.natap.org/2005/ias/ias_52.htm

18.     Hepatitis C infection is not associated with systemic HIV-associated
non-Hodgkin's lymphoma: a cohort study (09/09/05)
http://www.natap.org/2005/ias/ias_51.htm

19.     PI & NNRTI Drug Levels in Coinfected Patients (09/09/05)
http://www.natap.org/2005/ias/ias_50.htm

20.     Pegasys/RBV Improves Histology in Non-Responders & Cirrhotics
(09/09/05)
http://www.natap.org/2005/ias/ias_49.htm

21.     PegIFN/RBV May Be Less Effective in Acute HCV for HIV+ (09/09/05)
http://www.natap.org/2005/ias/ias_48.htm

22.     PK of Once Daily Regimen: Fosamprenavir/r, Tenofovir and FTC in
Naives (09/09/05)
http://www.natap.org/2005/ias/ias_47.htm

23.     Occult HCV- HCV RNA Found in Liver of Patients Negative for
Antibody-HCV & Serum HCV RNA - (09/05/05)
http://www.natap.org/2005/HCV/090505_20.htm

24.     EDITORIAL COMMENTARY Hepatitis C Virus (HCV) Occult Infection or
Occult HCV RNA Detection? - (09/05/05)
http://www.natap.org/2005/HCV/090505_10.htm

25.     HCV Did Not Persist in Patients with SVR - (09/05/05)
http://www.natap.org/2005/HCV/090505_19.htm

26.     Divining the role of liver biopsy in hepatitis C - (09/05/05)
http://www.natap.org/2005/HCV/090505_18.htm

27.     Chronic hepatitis C and 'normal' ALT levels: Treat the disease not
the test - (09/05/05)
http://www.natap.org/2005/HCV/090505_17.htm

28.     Gilead, Achillion initiate phase I trial evaluating GS 9132 for
treatment of hep C - (09/05/05)
http://www.natap.org/2005/HCV/090505_16.htm

29.     Isatoribine, an agonist of TLR7, reduces plasma virus concentration
in chronic hepatitis C infection - (09/05/05)
http://www.natap.org/2005/HCV/090505_15.htm

If that's not enough for you there are 420 more articels posted at the
following URL;
http://www.natap.org/hcv.htm

Gary Stein
DavidT - 22 Sep 2005 13:40 GMT
You forget, Gary.
There is a massive global biomedicalconspiracy that has infiltrated
every single academic institute, every hospital and every research
laboratory. All employees are co-conspirators paid directly or
indirctly by BigPharma to create non-existent organisms and diseases.
Of course you will see thousands of studies on Hepatits C - but none of
them were really carried out, and all are fraudulent.
Iconoclaster - 25 Sep 2005 01:55 GMT
Paper #5 is very exciting.  To marketing people, that is, not to
scientists:

>"It is estimated that 170 million persons worldwide are chronically
infected with HCV, most of whom reside in developing nations and many of
whom may be coinfected with HIV and/or HBV and have very limited access to
treatment. Even if only 10% of such individuals advanced to cirrhosis, the
global burden of this infection is staggering.  Thus HCV, like HIV, is a
disease of two worlds, one where new infections are rare and effective
treatments are available and one where high population density, inadequate
preventive strategies and inaccessible treatments maintain HCV as a common
disease with devastating consequences."

Now if you read that, doesn't it give you an idea that there's money to be
made?
This "natural history of HCV" nowhere mentions when or where 'HCV' was
discovered or isolated.  It just enters the story unobtrusively.
Suddenly, it's there.
I agree with one point: HCV is like HIV.
Gary Stein - 25 Sep 2005 03:25 GMT
5 sets of personal opinions completely devoid of any discussion of facts
don't an argument make Herr Doctor Iconclaster....

Gary Stein

> Paper #5 is very exciting.  To marketing people, that is, not to
> scientists:
[quoted text clipped - 15 lines]
> Suddenly, it's there.
> I agree with one point: HCV is like HIV.
Iconoclaster - 25 Sep 2005 23:39 GMT
>"5 sets of personal opinions completely devoid of any discussion of facts
don't an argument make Herr Doctor Iconclaster....

Mr. Stein, do you really mean to say that this paper makes any kind of
argument?  The point we're discussing is the non-existance of HCV,
remember?

Iconoclaster - 27 Sep 2005 02:47 GMT
Paper #14   Is Cirrhosis Inevitable in HCV?

>"Remember, HIV can accelerate HCV progression up to 5 times more quickly
than in HCV monoinfection. It is generally accepted, as also reported from
this study, that HCV progresses slowly so if you live long enough
cirhhosis will develop. Therefore, HIV/HCV coinfection becomes a more
deadly disease. Many more coinfected patients appear to be at risk for
developing cirrhosis within a much shorter time than moninfected."

Oh sure!  I can believe that.  If you're deemed to be infected with HIV,
you get treated with HAART.     If you had liver trouble already, no
matter what caused it, HAART will finish you off.

>"......infection with HCV for over 60 years causes cirrhosis in 71% of
infected individuals. Because relationship between the severity of
fibrosis and age in Asian patients is similar to that seen in Caucasian
patients it is likely that similar rates of cirrhosis will be seen in
other patients who are infected for more than 60 years...."

Hey! This paper is fun! If you live long enough, you'll die of
something...

And now a word from our sponsor:

>"In summary, if the data gathered in the study are indeed a true
reflection of the long-term impact of chronic HCV infection among Asian
patients, and if the findings can be extended to other populations, this
would clearly indicate that substantially more, perhaps most, persons
infected with HCV are likely to reach end-stage liver disease than had
been thought hitherto. It also implies that treatment should indeed be
universal for all HCV-infected persons, regardless of their histologic
status, in the hope of blunting this progression.
In addition, it raises the issue of the need for even more transplantation
services to accommodate the anticipated (on the basis of this study)
"epidemic" of cirrhosis-related end-stage liver disease and cancer that
awaits these patients."

I guess the drug therapy and liver transplantation business will be
booming in the next 60 years.

So does HCV exist?  Who cares...
DavidT - 22 Sep 2005 13:41 GMT
You forget, Gary.
There is a massive global biomedicalconspiracy that has infiltrated
every single academic institute, every hospital and every research
laboratory. All employees are co-conspirators paid directly or
indirctly by BigPharma to create non-existent organisms and diseases.
Of course you will see thousands of studies on Hepatits C - but none of
them were really carried out, and all are fraudulent.
montygram - 22 Sep 2005 22:46 GMT
No conpiracy required.  There is little incentive to question existing
dogma, even if it was not properly established in the first place
(using controlled, double-blinded experiments, for example).

There are many scientific models that coexist, yet one must be correct,
or at least more accurate, than the other.  Those who don't examine the
points made by the Perth Group, for example, are not doing science,
which requires that all scientific challenges be taken seriously.  A
hypothesis is supposed to be scrutinized; otherwise, we would still
believe in a flat earth.

As an example of a what is going on all the time (though the public is
not aware of it), the following report is from TODAY.  There are
similar examples all over the place.  Go to www.gilbertling.org and
read about how he has tried to get funding for more experiments to
clarify his A-I hypothesis, but because a bureaucrat does not like him,
the experiments are not getting done.

Wake up and smell the coffee, people!

9/24/2005
"Sugar Helps Control Cell Division"

"...The dogma for decades has been that the cycle of cell division is
controlled by the appearance and disappearance of certain proteins
called cyclins, but experiments have shown that you can knock out any
of these and still get perfectly normal cell division..."

Source: www.sciencedaly.com

The other intesting thing is that there really is no "HIV/AIDS
hypothesis," because it varies from one period of time to another and
from one place to another.  Let's start with exactly what the
hypothesis is, otherwise, there can be no scientific debate.  Most
people in the USA (including doctors) think that after infection, a
person will live several years, perhaps a decade or so, then die of
"immune system failure," yet there is the following:

"Less than a quarter of HIV-positive men with haemophilia in the United
Kingdom are still alive 20-25 years after infection with HIV,"
So over 20% of people who are already very ill people can live over 25
years or so with HIV.

And then: "... liver disease has become the major cause of death
amongst HIV-positive men with haemophilia."

This is not an "AIDS defining illness," nor has anyone suggested it is.

How is this possible?  What is the hypothesis, exactly?

Source: Sabin C et al. Twenty five years of HIV in haemophilic men in
Britain: an observational study. BMJ, September 16th, 2005 (online
edition).

I have accepted my version of the Duesberg challenge, but nobody wants
to take me up on it, so they don't even believe in their own nonsense.

Then I asked, hypothetically, if someone did take me up on the
challenge, what would you inject me with?  I will only allow "pure
virus" and an inert susbstance in which to suspend the virus.  How are
you going to obtain this virus, since it was never isolated?  How will
you isolate it, exactly?  Explain it.  Only fragments, either of the
wrong size and right shape (according to the dogma, anyway) or of the
correct size and wrong shape, have ever been found, and they are most
likely from humans cells that destroyed in the massive oxidative stress
that actually does cause most of what is called "AIDS" these days (in
the USA, at least).

No conspiracy, just stupidity, fear of reprisals and loss of grants,
greed, etc. - all the things that make us human.

So take me up on the Duesberg challenge, or we could agreee upon a Hep
C challenge.  How, exactly, are you going to isolate this "Hep C
virus?"  If you beleive in a virus, isolate it and let's talk about
doing a experiment that will determine who is correct.  The problem, of
course, is that you cannot isolate what is not present.

Even true believers have to admit the nonsense, though they do it in a
quiet way:

"...the virus has not been grown in tissue culture. Thus, basic studies
of the virus are not possible and studies are limited to gene
sequencing and clinical studies. and clinical studies..."

Source: http://www.hepnet.com/hkn/c11.html

Do you people understand the implications of this?  Why can't they grow
it?  There is no reason, except that it does not exist!

They say: " The virus for hepatitis C was cloned in 1989," but what
does this mean, exactly?  Again, fragments were found that most likely
were part of human cells that underwent tremendous stress and died off.
These fragments were cloned and said to be "Hep C."  Why?  So that a
big company could make big money.  Does that surprise you?  Is it the
first example in human history of a company claiming something that is
not likely true in order to make huge profits?  Do you think everyone
in the company understand exactly what is going on at the molecular
level?  Let's be real now!  You are the ones with the naive view of
humanity.

The "studies" that allegedly support the virus claim are circular logic
- they assume a virus.  In science, you cannot assume what you seek to
demonstrate.  That is what religious debate is often like, for example,
assuming the Bible is the word of God, when there is no way to know
that scientifically.  So of course the studies will appear to support
the virus idea.  Do they compare this claim to an oxidative stress
hypothesis?  Find me a citation that answers that question.

I have confidence that I could "cure" "Hep C" in an animal model, but
these clowns admit that they have not been able to create one for "Hep
C," which is a damning statement by itself.  In people, we are dealing
with "patients" who have done tremendous damage to themselve, and who
usually don't listen to any authorities, let alone those who have no
power to enforce their demands (such as doctors), which is why I offer
myself up to demonstrate that this is all nonsense.  However, because
there is no virus, there is no way for anyone to take me up on my
offer, even if they were naive enough to do so.
GMCarter - 22 Sep 2005 23:30 GMT
>No conpiracy required.  There is little incentive to question existing
>dogma, even if it was not properly established in the first place
>(using controlled, double-blinded experiments, for example).

Hey, aren't you the guy that says no one should EVER even sniff an
omega-3 fatty acid?
David Canzi -- non-mailable - 23 Sep 2005 03:33 GMT
>Most
>people in the USA (including doctors) think that after infection, a
>person will live several years, perhaps a decade or so, then die of
>"immune system failure,"

The expectation for *U*N*T*R*E*A*T*E*D* people with HIV infection is
that about half develop AIDS within a decade.

>yet there is the following:
>
>"Less than a quarter of HIV-positive men with haemophilia in the United
>Kingdom are still alive 20-25 years after infection with HIV,"
>So over 20% of people who are already very ill people can live over 25
>years or so with HIV.

These people are being treated.

Signature

David Canzi            "I am not denying anything." -- Celia Farber

Lorenzo+ - 23 Sep 2005 14:22 GMT
> The expectation for *U*N*T*R*E*A*T*E*D* people with HIV infection is
> that about half develop AIDS within a decade.

Nobody remembers... conspiracies are more interesting!
Iconoclaster - 23 Sep 2005 00:44 GMT
Thank you, Mr. Stein, for presenting these 29 articles on Hep-C.  Hey!
That's neat:  One for every indicator disease of AIDS!  What a
coincidence!
Of course, I'll need a little time to study them, in order to find out
what's wrong with them.
There's no doubt, of course, that there IS something worng with them,
because Hep-C Virus doesn;'t exist.    There is no record of it being
isolated.  Some hepatic disease agency in this country informed me that
there are 9 classes of HCV and more than 100 subclasses.  But they gave me
absoluely zero information on the physical properties of this 'virus'  Not
even one puny subclass.
Of course they need this many different forms of the virus, because they
have to explain away all the different discrepancies of the virus model,
and one single virus type couldn't possibly do that.
There is another theory that explains all the deaths from liver disease
very well:  Hepatic damage from all the toxic drugs that are being used to
fight that other non-existing virus: HIV.
HCV is the "Alibi Virus", so to speak.
But don't go away; I'll be back when I've read those papers.
Iconoclaster - 24 Sep 2005 19:57 GMT
Oh puhlease!!  Here comes Paper #1:

>"These Phase 1 studies investigate SCH 503034 from Schering Plough both
as monotherapy and in combination with PEG-Intron in genotype 1 patients
who were nonresponders to peginterferon + ribavirin combination therapy.
It is important to note that these Phase 1 studies were conducted with a
capsule formulation that is viable for larger-scale clinical studies and,
potentially, for commercial development."

It says nothing about Hep-C, the virus.  It just ASSUMES that's the
problem.  Schering Plough is plotting a new poison, to be used on hapless
patients who have already been half-killed by peginterferon+ribavirin.  
Ribavirin is a terrible toxin.  It's main side effect is hemolytic anemia
(= forced apaoptosis of red blood cells)  Brrrrr!
Iconoclaster - 25 Sep 2005 01:10 GMT
Tadaaaaa!  Her comes paper #2:

>"All patients also received open-label lamivudine (150 mg twice daily
(3TC, Epivir) and stavudine (40 mg twice daily [d4T, Zerit]; patients
weighing <60 kg received 30 mg). All subjects were screened for HCV by
means of an HCV ELISA. Seventy (11%) of 653 subjects enrolled in the
parent clinical trial were HCV-antibody reactive upon HCV ELISA testing.

".....this analysis confirms that HCV loads increase after HAART
initiation and that this increase is associated with appropriate immune
reconstitution. These increases may be accompanied by flares in the ALT
level."

<Sob!>  The same old sh.t as with 'HIV' !  Testing with ELISA, this time
with proteins ASSUMED to come from 'HCV'.  Also Viral Load testing while
at the same time murdering the patient with lamivudine and stavudine.

Any evidence of Hep-C Virus?  I'm not seeing it.
GMCarter - 25 Sep 2005 12:33 GMT
snip

><Sob!>  The same old sh.t as with 'HIV' !  Testing with ELISA, this time
>with proteins ASSUMED to come from 'HCV'.  Also Viral Load testing while
>at the same time murdering the patient with lamivudine and stavudine.
>
>Any evidence of Hep-C Virus?  I'm not seeing it.

You haven't looked for it and wouldn't know what to do if the evidence
was staring you in the face. At best, you live in a world of
technology that has not gotten passed about 1938.

NOTHING in ANY of your posts suggests that your unsujpported opinion
should be given more attention than a rat's fart.

        George M. Carter
Iconoclaster - 25 Sep 2005 23:43 GMT
>"NOTHING in ANY of your posts suggests that your unsujpported opinion
should be given more attention than a rat's fart."

Not by you, Mr. Carter.  But surely by people who are able to think for
themselves.  You only have to read this paper to seen that it presents
absolutely no evidence in favor of the existance of HCV.
GMCarter - 26 Sep 2005 14:37 GMT
>>"NOTHING in ANY of your posts suggests that your unsujpported opinion
>should be given more attention than a rat's fart."
>
>Not by you, Mr. Carter.  But surely by people who are able to think for
>themselves.  You only have to read this paper to seen that it presents
>absolutely no evidence in favor of the existance of HCV.

So says you based on nothing but your ill-considered opinion.
Iconoclaster - 25 Sep 2005 01:24 GMT
Paper #3 is about monotherapy with Peginterferon a-2b:

>"Results: Five untreated subjects had spontaneous recovery and another 4
subjects scheduled to start treatment at weeks 12 or 20 resolved
spontaneously before therapy. 79 subjects with persistent viremia were
randomized to 3 groups (Table). The end of treatment response was 94% and
the overall SVR was 82%. The SVR was better for genotype 4 compared to
genotype 1. Earlier treatment (week 8 or 12) was associated with higher
SVR particularly in genotype 1. Twelve week therapy was sufficient for
genotype 4 while higher SVR rates in genotype 1 patients were achieved
with 24 wks treatment (86%). Peginterferon c~-2b monotherapy was well
tolerated and associated with significant improvement in the quality of
life."

These genotypes depend on what kind of genetic sludge has been used to
prime the PCR.
Peginterferon a-2b is well-tolerated.  As a monotherapy it will not kill
you as easily as in combination with Ribavirin.  I can believe that.
But just waiting until the condition clears up by itself, as happened to 9
subjects, works too.


Iconoclaster - 25 Sep 2005 01:45 GMT
Paper #4:

>"Background/Aims: Hypermetabolism is considered to be of clinical
interest in liver disease and in several chronic viral infections. Whether
resting energy expenditure (REE) increases during chronic hepatitis C is
not known. Our aims were: (a) to determine the metabolic state of patients
with chronic hepatitis C, and (b) to evaluate the effects of interferon
therapy on REE.

Well, this study came out the same way it always happens in the clinic:
Some patients respond to treatment, other patients don't.

But wait: The authors claim that the REE is really caused by the virus
(HCV):

>"As increased REE was correlated with the virus load but not with
histological status or ALT activity, hypermetabolism might be a direct
result of HCV replication rather than the consequence of hepatic
inflammation."

Yeah, it might...  Now if we could only prove that there IS a virus...
Hm! Viral load, eh?  Isn't that based on quantitative PCR?  What did kary
Mullis have to say about that?
Iconoclaster - 26 Sep 2005 00:07 GMT
Paper #6: (Marijuana/Hash) Endocannabinoids and liver disease - review -

Well, this paper is exactly what the title says it is. But... NOT A WORD
ON HCV, or any virus at all.
It does contain the following stement:

>"These results suggest that chronic marijuana use, alone or in
combination with alcohol or other drugs, may have hepatotoxic effects"

Ouch!  That will take away the chance for hippies and other babyboomers to
blame all the mysery on some real or imagined virus.
GMCarter - 26 Sep 2005 14:33 GMT
>Paper #6: (Marijuana/Hash) Endocannabinoids and liver disease - review -
>
[quoted text clipped - 7 lines]
>Ouch!  That will take away the chance for hippies and other babyboomers to
>blame all the mysery on some real or imagined virus.

Ah...alcohol impairs liver function depending on the dose and duration
of use. The hepatotoxicity of marijuana is hardly confirmed by this
study; the evidence for it is weak at best.

Alcohol and marijuana do not cause AIDS. Alcohol may of course cause
cirrhosis. You think it's just the same as HCV-related cirrhosis,
histopathologically  speaking?

        George M. Carter
Iconoclaster - 27 Sep 2005 01:22 GMT
>"Alcohol and marijuana do not cause AIDS. Alcohol may of course cause
cirrhosis. You think it's just the same as HCV-related cirrhosis,
histopathologically  speaking?"

No, for two reasons:
1. Cirrhosis i not the same as hepatitis
2. HCV-related cirrhosis or HCV-anything does not exist.
There are many ways to screw up your liver, but a non-existent virus is
not one of them.
Most kinds of liver damage are caused by toxic chemicals.
Iconoclaster - 26 Sep 2005 00:30 GMT
Paper #7:  Impact of Hepatitis C Virus on Immune Restoration in
HIV-Infected Patients Who Start Highly Active Antiretroviral Therapy: A
Meta-analysis -

This is indeed a Meta-analysis, i.e., a literature search and comparison
of a number of papers on the subject.  The authors note:

>"This meta-analysis is dependent on the published literature, and the
studies reviewed are very different in their design. In all of the
studies, the increase in the CD4 cell count was a secondary outcome, and
many of the studies are statistically underpowered to examine the specific
question of interest to us."

Nevertheless, the conclusion of this study is:

>"This meta-analysis shows that patients with HIV-HCV coinfection do, in
fact, have less immune reconstitution, as determined by CD4 cell count
after 48 weeks of HAART, than do patients with HCV infection alone. "

The auhors don't come up with an explanation of this phenomenon.
My objection is that, again, "HCV infection" is taken for granted.  Like
"HIV infection" it is based on an antibody test.  As there is no standard
in the form of a pure HCV preparation (if there were, they would have
cited a reference), the term "HCV infection" has no real meaning.
Iconoclaster - 26 Sep 2005 00:42 GMT
Paper #8: Hepatitis C Virus Infection in HIV Type 1-Infected Individuals
Does Not Accelerate a Decrease in the CD4+ Cell Count but Does Increase
the Likelihood of AIDS-Defining Events

Well, the title says it all, now doesn't it?
If you've tested HIV+, you croak sooner if your liver is screwed up too,
and CD4+ cells have nothing to do with that.  The paper states:

>"In conclusion, there was an increased number of adverse events in
coinfected individuals, compared with individuals infected with HIV-1
alone."

Note that these patients were treated with HAART.  Their CD4+ cells went
up, but they died anyway of liver disease.  This is a very clear example
where they sorely need another fantasy virus (HCV) to explain this
outcome!
GMCarter - 26 Sep 2005 14:39 GMT
>Note that these patients were treated with HAART.  Their CD4+ cells went
>up, but they died anyway of liver disease.  This is a very clear example
>where they sorely need another fantasy virus (HCV) to explain this
>outcome!

So it is your belief that all antiretrovirals used to treat HIV are
hepatotoxic.
Iconoclaster - 27 Sep 2005 01:25 GMT
>"So it is your belief that all antiretrovirals used to treat HIV are
hepatotoxic."

Not necessarily.  But Proteinase Inhibitors are.
GMCarter - 27 Sep 2005 12:11 GMT
>>"So it is your belief that all antiretrovirals used to treat HIV are
>hepatotoxic."
>
>Not necessarily.  But Proteinase Inhibitors are.

Really. All of them. "Proteinase"?

Wow. You're arrogance and hubris are stunning in the breadth and scope
of absolutely nothing they have to back them.

You give W a run for his money.

        George M. Carter
Iconoclaster - 28 Sep 2005 01:36 GMT
>"Really. All of them. "Proteinase"?

Yes, Mr. Carter.  All Protease Inhibitors (excuse the misspelling.  It was
late at night.

And by the way, It's not a 'run for the moey'.  I'm having a field trip,
or a field day, or whatever.
And you, Mr. Carter... are grasping at straws.
GMCarter - 28 Sep 2005 11:46 GMT
>>"Really. All of them. "Proteinase"?
>
>Yes, Mr. Carter.  All Protease Inhibitors (excuse the misspelling.  It was
>late at night.

Why? You're supposed to be the educated expert, aren't you?

I forgive you nothing.
Iconoclaster - 29 Sep 2005 01:13 GMT
>"Why? You're supposed to be the educated expert, aren't you?  I forgive
you nothing."

They didn't have Protease Inhibitors in 1938.  They did have good science,
though.
GMCarter - 29 Sep 2005 12:18 GMT
>>"Why? You're supposed to be the educated expert, aren't you?  I forgive
>you nothing."
>
>They didn't have Protease Inhibitors in 1938.  They did have good science,
>though.

And nothing has changed in 67 years in science? remarkable.
Iconoclaster - 29 Sep 2005 22:52 GMT
>"And nothing has changed in 67 years in science? remarkable."

But a lot has changed in science, Mr. Carter!  Mainly the scientists.
They were not so corrupt back then.  And science was not big-money
business then either.
GMCarter - 30 Sep 2005 13:08 GMT
>>"And nothing has changed in 67 years in science? remarkable."
>
>But a lot has changed in science, Mr. Carter!  

You bet. Pity you didn't bother to keep up with ANY of it.
Gary Stein - 03 Oct 2005 19:24 GMT
> >"And nothing has changed in 67 years in science? remarkable."
>
> But a lot has changed in science, Mr. Carter!  Mainly the scientists.
> They were not so corrupt back then.  And science was not big-money
> business then either.

Oh please science has always been about money or power or both. Most
progress in science can be attributed to war and conflict. Progress in
Medicine is of course extremely linked to warfare. The idea that it is
otherwise is the result of rationalization on the part of scientists for the
most part.

Gary Stein
pauleewhiting - 03 Oct 2005 22:13 GMT
"Oh please science has always been about money or power or both. Most
progress in science can be attributed to war and conflict. Progress in
Medicine is of course extremely linked to warfare. The idea that it is
otherwise is the result of rationalization on the part of scientists for
the most part."

And let me guess, Gary, you think that this history of science being
"about money or power or both" somehow *doesn't* apply to the HIV theory
of AIDS, right?

And that the "idea that it is otherwise is the result of rationalization
on the part of scientists" *doesn't* apply to the AIDS scientists, right?
Gary Stein - 04 Oct 2005 20:09 GMT
> "Oh please science has always been about money or power or both. Most
> progress in science can be attributed to war and conflict. Progress in
[quoted text clipped - 8 lines]
> And that the "idea that it is otherwise is the result of rationalization
> on the part of scientists" *doesn't* apply to the AIDS scientists, right?

You are a dimwit aren't you Paul, of course what I said applies, however it
has nothing to do with HIV=AIDS or the validity of the clinical data that
backs up that statement. It is simply a fact of life in this world and
science seems to have dealt with it pretty effectively or we would still be
bleeding folks and drilling holes in heads to release foul spirits which
both make as much sense as claiming HIV is harmless.

Gary Stein
pauleewhiting - 04 Oct 2005 22:03 GMT
"...of course what I said applies, however it has nothing to do with
HIV=AIDS or the validity of the clinical data that backs up that
statement."

Just like I said, Gary, "science has always been about money or power or
both" with the one exception, of course, being the HIV theory of AIDS...
GMCarter - 05 Oct 2005 00:26 GMT
>"...of course what I said applies, however it has nothing to do with
>HIV=AIDS or the validity of the clinical data that backs up that
>statement."
>
>Just like I said, Gary, "science has always been about money or power or
>both" with the one exception, of course, being the HIV theory of AIDS...

And also about discovery, health, hubris, arrogance--and all the
various motivators of human beings.

So what?

This does NOT mean HIV does not exist or cause AIDS any more than
cancer exists and causes disease. Or heart problems.

Does it have other consequences? You bet it does.

        George M. Carter
pauleewhiting - 05 Oct 2005 02:24 GMT
And also about discovery, health, hubris, arrogance--and all the various
motivators of human beings.

So what?

This does NOT mean HIV does not exist or cause AIDS any more than cancer
exists and causes disease. Or heart problems.

Does it have other consequences? You bet it does."

Yes, like people being given a terminal diagnosis based on non-specific
anti-body tests, which are known to be highly cross-reactive.

And the results from those tests are then interpreted based on whether the
patient belongs to a known "risk group."

That's why part of HIV testing includes a questionnaire to determine
whether you fall into a known "risk group."

Thus, if you're Elisa and Western Blot tests come back positive and you're
gay, you are determined to be HIV-positive based soley on the fact you are
part of a "risk group" whose known "high-prevalencey of HIV infection"
lends itself to your HIV diagnosis...

It's one of the finest examples of circular logic known to mankind.
wilyretrovirus - 05 Oct 2005 03:11 GMT
Here's the formula.  

You test "positive" on a non-specific antibody test because you're in a
"high-risk group".

You're in a "high-risk group" because you test "positive" on a
non-specific antibody test.

Where do I sign up?

BTW, George, I'm *still* waiting to meet my very first heterosexual
caucasian male diagnosed "HIV-positive".  
GMCarter - 05 Oct 2005 12:38 GMT
snip
>Yes, like people being given a terminal diagnosis based on non-specific
>anti-body tests, which are known to be highly cross-reactive.

The Ab tests are very specific and NOT highly cross-reactive. See the
other threads. This is an unsupported lie.

>And the results from those tests are then interpreted based on whether the
>patient belongs to a known "risk group."

As part of the overall diagnosis, yes.

>That's why part of HIV testing includes a questionnaire to determine
>whether you fall into a known "risk group."
[quoted text clipped - 3 lines]
>part of a "risk group" whose known "high-prevalencey of HIV infection"
>lends itself to your HIV diagnosis...

I see. That's the answer you want and that works for you. Evidence to
the contrary notwithstanding.

That's fine, dear. You go with that. You can believe whatever nonsense
you like. So!

What's your creation myth look like? A big white guy with a beard
dithering about in the dark til he lights a match? An infinite layer
of turtles?

        George M. Carter
pauleewhiting - 06 Oct 2005 04:48 GMT
"And the results from those tests are then interpreted based on whether the
patient belongs to a known 'risk group.'

As part of the overall diagnosis, yes."
pauleewhiting - 06 Oct 2005 04:52 GMT
"This is an unsupported lie."

"Chemo does NOT cause CD4 cells to drop. They may cause other problems,
like anemia. But that ain't a drop in CD4 count, etc."

"Chemotherapy can make you more likely to get infections. This happens
because most anticancer drugs affect the bone marrow, making it harder to
make white blood cells (WBCs), the cells that fight many types of
infections."
Iconoclaster - 26 Sep 2005 00:57 GMT
Paper #9:  VA Study: HCV Increases Risk of Death Among HAART-Treated HIV+
Patients by 30-80%

More of the same.  

Our analysis showed>" that HCV infection increases the risk of death in
HIV patients who received HAART, controlling for numerous demographic and
clinical factors, including exposure to HAART and response to HAART.
Depending on the factors for which we controlled, we found that the risk
of death among HAART-treated HIV patients was between 30% and 80% higher
for those also infected with HCV."

With the same right, we could say that the risk of death is increased by
HAART.  We don't need 'HCV' in the equation.  No evidence is presented, of
course, that it exists.  They just ASSUME it's there.
Iconoclaster - 26 Sep 2005 01:13 GMT
Paper #10:  Influence of Hepatitis C Virus Infection on HIV-1 Disease
Progression and Response to Highly Active Antiretroviral Therapy"

This paper covers the same subject as paper #8.
here is the main conclusion:

>" Conclusions. HCV serostatus did not affect the risk of HIV-1 disease
progression, but the risk of liver disease-related deaths was markedly
increased in HCV-seropositive patients. The overall virologic and
immunologic responses to HAART were not affected by HCV serostatus."

Well now, that doesn't pull any punches, now does it?  If you take HAART,
you don't die of AIDS.  You die of liver disease instead!  Now doesn't
that make you feel better?
Iconoclaster - 27 Sep 2005 01:46 GMT
Paper #11:  This paper aims at contradicting an earlier report (by other
researchers) about stavudine and several other drugs causing steatosis.

>"We then focused on the use of stavudine in particular. Steatosis was
observed in 53% of patients who had ever used stavudine (n = 51, mean
grade 1.1, range 0-4), compared with the identical prevalence of steatosis
(53%) in patients who had never used stavudine"

The reviewer, Jules Levin, notes:
"Although study did not find difference between groups described above
regarding incidence of steatosis, they did not look at patients separately
who had glucose and lipid abnormalities, risk factors for steatosis.
Although the differences below were not statistically significant, the
number of patients in the study was small."

Actually, a fatty liver can have many causes.
To list a few:

   1. Obesity.
   2. Alcohol.
   3. Diabetes.
   4. Medications like hormones, steroids, heart       medications etc.
   5. Several uncommon diseases of fat and carbohydrate metabolism.
   6. Several diseases of the pancreas and intestines, all uncommon.
   7. Malnutrition.
   8. Other diseases.

"HCV" is taking a backseat here.  It's a drug study.
Iconoclaster - 27 Sep 2005 02:01 GMT
Paper #12:  Promising Therapy for Human Hepatoma (liver cancer, HCC):
Telomerase

I don't really have anything againt this paper, but... it deals with liver
cancer chemotherapy:

>"Telomerase antagonists GRN163 and GRN163L inhibit tumor growth and
increase chemosensitivity of human hepatoma"

Very interesting.  But not a WORD about "HCV"  (and rightfully so).
Iconoclaster - 27 Sep 2005 02:29 GMT
Paper #13:  Single (B or C), dual (BC or BD) and triple (BCD) viral
hepatitis in HIV-infected patients in Madrid, Spain

>"Hepatitis was classified as follows: HB, positive serum HBsAg and
negative serum HCV and HDV antibodies; HC, positive HCV antibodies and
negative HBsAg; HBC, positive HBsAg, positive HCV antibodies and negative
HDV total antibodies; HBD, positive HBsAg, positive total HDV antibodies
and negative HCV antibodies; HBCD, positive HBsAg, positive HCV antibodies
and positive total HDV antibodies."

Sí caballeros, those wily Spanyards have invented a Hep-D virus.  Occurs
only in Spain and Portugal, so far, but export to South-America is being
considered.  Obviously, there are data that cannot even be explained away
with Hep-C, so they just came up with another one.
You will notice from the quote above that all the tests are serological.
They just say: These proteins are from HCV, and those are from HDV, and
we're all supposed to believe that.
I tend to believe in HBV, because I've actually seen evidence for the
existence of Hep-B virus.  But Hep-C, not to mention Hep-D...  No evidence
at all, and certainly not in this paper.
Iconoclaster - 27 Sep 2005 03:16 GMT
Paper #15   Insulin resistance is a cause of steatosis and fibrosis
progression in chronic hepatitis C

Did you ever play poker with your old-maid aunt?  Lots of variants with
Wild Cards.  You can build any winning hand, using them.  Well, HCV is
such a Wild Card.  You can invoke it any time you can't make heads or
tails of the data:

>"The relationship between steatosis and fibrosis could be explained by
several other mechanisms, such as lipid peroxidation.38-41 According to
the "two hits hypothesis", steatosis could increase the sensitivity of
hepatocytes to oxidative stress, the second hit being HCV infection itself
in patients with chronic hepatitis C.39 Production of reactive oxygen
species in an in vitro model expressing HCV core protein is consistent
with this hypothesis."

Right.  They just point a finger at a protein and say: "Tis is HCV core
protein."  But, just as in the case of 'HIV', there is no virus particle
to check it against.

We're halfway through the 29 papers now, Mr. Stein.  If the other half is
just like the first half, I'll be seriously pissed.
robinhvd - 27 Sep 2005 06:46 GMT
Iconoclaster, how can they not be as pointless as the first half -- look at
the dates!? Please let us know if you find at least references to the
seminal publications announcing the existence of HCV -- i.e. the Gallo
papers of HCV. Happy reading.
Iconoclaster - 29 Sep 2005 20:48 GMT
Paper #16:  Hepatocellular carcinoma in 40 HIV/HCV-coinfected versus 50
HCV-monoinfected patients.

Whoever thinks that Mr. Stein's 29 papers are all peer-reviewed journal
articles, better think again.  This paper was presented at the
International AIDS Conference in Rio de Janeiro, this summer.  And it's a
scream!

>"Only 1 of 90 patients was female. HIV/HCV patients were younger than HCV
patients, and they consumed less alcohol."

In other words:  The "HCV patients were old enough to have screwed up
their liver with alcohol"  The younger ones were told they were also
infected with HIV, so their livers were destroyed with HAART.

>"Time from initial HCV infection to HCC was 7.5 years shorter in HIV/HCV
compared to HCV patients (26.4 yrs, n=30, vs 35.2 yrs, n=62)."

(HCC =Hepatic Cellular Carcinoma)
So it takes much less time to cancerize you liver with HAART than with any
other toxic substance (such as alcohol or Tylenol).

>"Conclusions: HIV/HCV-coinfected patients develop HCC at a younger age
than HCV-monoinfected patients due to a shorter interval from HCV
infection to HCC. In contrast to the European study, we did not find a
difference in survival between HIV/HCV and HCV patients."

As I mentioned already, Treatment for HIV (although they don't mention it)
leads to liver cancer sooner that anything else.
Of course there is no difference in survival:  You have only one liver.
And when you screw it up, you've had it.

This paper had no less than 13 (!) authors.  Now be honest: Are my
explanations in straight, simple language not far superior over the
contrived hoopla of these 13 'experts'?
Iconoclaster - 29 Sep 2005 21:48 GMT
Paper #17:  Caucasians Had Better HCV Viral Load Reductions Than
African-Americans During First 3 Days & During Weeks 1-4 After Starting
Peg/RBV

Here they measure the difference in 'viral kinetics' between white and
black people.  The viruses (HIV and HCV)are measured as Viral Load.  Of
course the existence of these viruses never comes into play. They just
have 2 jars with RNA snippets.  One says: "This be HCV", and the other:
"We call this HIV".  They use them for PCR, so they can measure 'Viral
Load'.  And this VL goes down whenth patients are treated with PEGLFN and
that frightening stuff, Ribavirin.
And guess what?  The Caucasians get their VL down to nothing faster than
the Afro-Americans.
Ideas anyone?
Iconoclaster - 29 Sep 2005 21:55 GMT
Paper #18:  Hepatitis C infection is not associated with systemic
HIV-associated non-Hodgkin's lymphoma: a cohort study

>"Conclusions: In this immunocompromised patient population, there was no
association between HCV infection and an increased risk of lymphoma."

Ah!  The good news is that there's no bad news.  And the bad news is that
that's all the good news there is.

>"ED NOTE from Jules Levin: this is an important question and so we need
better designed studies to tease out the possibility that HCV & HIV may
cause higher rates of NHL in certain HIV+ patient populations."

Yeah.  Better studies.  I'm all for that.
Iconoclaster - 29 Sep 2005 22:33 GMT
Paper #19:  PI & NNRTI Drug Levels in Coinfected Patients

>"The study authors found that In HCV/HIV coinfected patients in this
study Cmin "did not change significantly' for lopinavir, but the authors
said NNRTIs "were strongly overdosed" in coinfected patients suggesting
the need for drug monitoring in this population."

The cart before the horse.  Is there really nobody who thinks of the
posibility that high doses of NNRTIs cause liver damage, so that they have
to postulate a virus (HCV) to blame for the damage?
In other words, if you're already 'infected' with HIV (accoding to
folklore), you become automatically 'co-infected' with HCV.
Iconoclaster - 29 Sep 2005 22:49 GMT
Paper #20:  Pegasys/RBV Improves Histology in Non-Responders & Cirrhotics

This is nothing but a clinical drug trial on patients with a bum liver.
Not a word about HCV (oh well, why should there be?).
The main conclusion is that COPEGUS (= ribavirin, the poison from hell) is
so good.
I wonder who financed this study...
GMCarter - 30 Sep 2005 13:02 GMT
>Paper #20:  Pegasys/RBV Improves Histology in Non-Responders & Cirrhotics
>
>This is nothing but a clinical drug trial on patients with a bum liver.

Bullshit. This is what I mean. This cannot be passed off as an
"analysis."

It is merely you spewing an unfounded and unqualified opinion.

        George M. Carter
 
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